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Jérémy Di Domizio, Muhammet Fatih Gulen, Fanny Saidoune, Vivek V. Thacker, Ahmad Yatim, Kunal Sharma, Théo Nass, Emmanuella Guenova, Martin Schaller, Curdin Conrad and 7 more
COVID-19, which is caused by infection with SARS-CoV-2, is characterized by lung pathology and extrapulmonary complications 1,2 . Type I interferons (IFNs) have an essential role in the pathogenesis of COVID-19 (refs 3–5 ). Although rapid induction of type I IFNs limits virus propagation, a sustained increase in the levels of type I IFNs in the late phase of the infection is associated with aberrant inflammation and poor clinical outcome 5–17 . Here we show that the cyclic GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway, which controls immunity to cytosolic DNA, is a critical driver of aberrant type I IFN responses in COVID-19 (ref. 18 ). Profiling COVID-19 skin manifestations, we uncover a STING-dependent type I IFN signature that is primarily mediated by macrophages adjacent to areas of endothelial cell damage. Moreover, cGAS–STING activity was detected in lung samples from patients with COVID-19 with prominent tissue destruction, and was associated with type I IFN responses. A lung-on-chip model revealed that, in addition to macrophages, infection with SARS-CoV-2 activates cGAS–STING signalling in endothelial cells through mitochondrial DNA release, which leads to cell death and type I IFN production. In mice, pharmacological inhibition of STING reduces severe lung inflammation induced by SARS-CoV-2 and improves disease outcome. Collectively, our study establishes a mechanistic basis of pathological type I IFN responses in COVID-19 and reveals a principle for the development of host-directed therapeutics.
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Domizio, J. D., Gulen, M. F., Saidoune, F., Thacker, V. V., Yatim, A., Sharma, K., Nass, T., Guenova, E., Schaller, M., Conrad, C., Goepfert, C., Leval, L. D., Garnier, C. V., Berezowska, S., Dubois, A., Gilliet, M. F., & Ablasser, A. (2022). The cGAS–STING pathway drives type I IFN immunopathology in COVID-19. Nature, 603(7899), 145–151. https://doi.org/10.1038/s41586-022-04421-w
Domizio, Jérémy Di, et al. "The cGAS–STING pathway drives type I IFN immunopathology in COVID-19." Nature, vol. 603, no. 7899, 2022, pp. 145–151, https://doi.org/10.1038/s41586-022-04421-w.
Domizio, Jérémy Di, Muhammet Fatih Gulen, Fanny Saidoune, Vivek V. Thacker, Ahmad Yatim, Kunal Sharma, Théo Nass, et al. "The cGAS–STING pathway drives type I IFN immunopathology in COVID-19." Nature 603, no. 7899 (2022): 145–151. https://doi.org/10.1038/s41586-022-04421-w.
Domizio J. D., Gulen M. F., Saidoune F. [и др.] The cGAS–STING pathway drives type I IFN immunopathology in COVID-19 // Nature. — 2022. — Vol. 603, № 7899. — P. 145–151. — URL: https://doi.org/10.1038/s41586-022-04421-w
@article{domizio2022cgassting,
title = {{The cGAS–STING pathway drives type I IFN immunopathology in COVID-19}},
author = {Jérémy Di Domizio and Muhammet Fatih Gulen and Fanny Saidoune and Vivek V. Thacker and Ahmad Yatim and Kunal Sharma and Théo Nass and Emmanuella Guenova and Martin Schaller and Curdin Conrad and Christine Goepfert and Laurence de Leval and Christophe von Garnier and Sabina Berezowska and Anaëlle Dubois and Michel F. Gilliet and Andrea Ablasser},
journal = {Nature},
year = {2022},
volume = {603},
number = {7899},
pages = {145--151},
doi = {10.1038/s41586-022-04421-w},
url = {https://doi.org/10.1038/s41586-022-04421-w}
}TY - JOUR AU - Domizio, Jérémy Di AU - Gulen, Muhammet Fatih AU - Saidoune, Fanny AU - Thacker, Vivek V. AU - Yatim, Ahmad AU - Sharma, Kunal AU - Nass, Théo AU - Guenova, Emmanuella AU - Schaller, Martin AU - Conrad, Curdin AU - Goepfert, Christine AU - Leval, Laurence de AU - Garnier, Christophe von AU - Berezowska, Sabina AU - Dubois, Anaëlle AU - Gilliet, Michel F. AU - Ablasser, Andrea TI - The cGAS–STING pathway drives type I IFN immunopathology in COVID-19 JO - Nature VL - 603 IS - 7899 SP - 145 EP - 151 PY - 2022 DA - 2022/01/19 DO - 10.1038/s41586-022-04421-w UR - https://doi.org/10.1038/s41586-022-04421-w ER -
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